When Mark Martindale decided to trace the evolutionary origin of muscle cells, like the ones that form our hearts, he looked in an unlikely place: the genes of animals without hearts or muscles.

In a new study published in the journal Proceedings of the National Academy of Sciences, the University of Florida scientist and colleagues found genes known to form hearts cells in humans and other animals in the gut of a muscle-less and heartless sea anemone. But the sea anemone isn't just any sea creature. It has superpower-like abilities: Cut it into many pieces and each piece will regenerate into a new animal.

So why does the sea anemone regenerate while humans cannot? When analyzing the function of its "heart genes," study researchers discovered a difference in the way these genes interact with one another, which may help explain its ability to regenerate, said Martindale, a UF biology professor and director of the Whitney Lab for Marine Bioscience in St. Augustine.

The study's findings point to potential for tweaking communication between human genes and advancing our ability to treat heart conditions and stimulate regenerative healing, he said.

"Our study shows that if we learn more about the logic of how genes that give rise to heart cells talk to each other, muscle regeneration in humans might be possible," Martindale said.

These heart genes generate what engineers calls lockdown loops in vertebrates and flies, which means that once the genes are turned on, they tell each other to stay on in an animal's cells for its entire lifetime. In other words, animals with a lockdown on their genes cannot grow new heart parts or use those cells for other functions.

"This ensures that heart cells always stay heart cells and cannot become any other type of cell," Martindale said.

But in sea anemone embryos, the lockdown loops do not exist. This finding suggests a mechanism for why the gut cells expressing heart genes in sea anemones can turn into other kinds of cells, such as those needed to regenerate damaged body parts, Martindale said.

The study supports the idea that definitive muscle cells found in the majority of animals arose from a bifunctional gut tissue that had both absorptive and contractile properties. And while the gut tissue of a sea anemone might not look like a beating heart, it does undergo slow, rhythmic peristaltic waves of contraction, much like the human digestive system.

Study authors argue that the first animal muscle cells might have been very heart-like, Martindale said.

"The idea is these genes have been around a long time and preceded the twitchy muscles that cover our skeleton," Martindale said.

Continued research could one day allow scientists to coax muscles cells into regenerating different kinds of new cells, including more heart cells, Martindale said

Sleep loss increases the risk of obesity through a combination of effects on energy metabolism. This research, presented at the European Congress of Endocrinology in Lisbon, will highlight how disrupted sleep patterns, a common feature of modern living, can predispose to weight gain, by affecting people’s appetite and responses to food and exercise.

In the 24/7 culture of the modern world, an increasing number of people report routine reduced quality of sleep and several studies have correlated sleep deprivation with weight gain. The underlying cause of increased obesity risk from sleep disruption is unclear but may relate to changes in appetite, metabolism, motivation, physical activity or a combination of factors.

Dr Christian Benedict from Uppsala University, Sweden and his group have conducted a number of human studies to investigate how sleep loss may affect energy metabolism. These human studies have measured and imaged behavioural, physiological and biochemical responses to food following acute sleep deprivation. The behavioural data reveal that metabolically healthy, sleep-deprived human subjects prefer larger food portions, seek more calories, exhibit signs of increased food-related impulsivity, experience more pleasure from food, and expend less energy.

The group’s physiological studies indicate that sleep loss shifts the hormonal balance from hormones that promote fullness (satiety), such as GLP-1, to those that promote hunger, such as ghrelin. Sleep restriction also increased levels of endocannabinoids, which is known to have appetite-promoting effects. Further work from Dr Benedict’s team shows that acute sleep loss alters the balance of gut bacteria, which has been widely implicated as key for maintaining a healthy metabolism. The same study also found reduced sensitivity to insulin after sleep loss.

Dr Christian Benedict remarks, “Since perturbed sleep is such a common feature of modern life, these studies show it is no surprise that metabolic disorders, such as obesity are also on the rise.”

Although Dr Benedict’s work has shed light on how short periods of sleep loss can affect energy metabolism, longer-term studies are needed to validate these findings. The group are now investigating longer-term effects and also whether extending sleep in habitual short sleepers can restore these alterations in appetite and energy metabolism.

Dr Christian Benedict says, “My studies suggest that sleep loss favours weight gain in humans. It may also be concluded that improving sleep could be a promising lifestyle intervention to reduce the risk of future weight gain.”

New research uncovers unexpected links between sleep deprivation and pain sensitivity. The findings may have significant implications for pain management therapies.

A recent study from the National Institutes of Health (NIH) estimates that more than 25 million adults in the United States live with chronic pain, and almost 40 million adults have experienced severe pain in the past 3 months.

Any pain that lasts for longer than 12 weeks is considered to be chronic. Chronic pain can be a consequence of injury, an underlying illness, or it may have no known cause.

Many people resort to complementary medical practices such as yoga or meditation to ease the pain. New research, however, examines the link between sleep deprivation, pain sensitivity, and common painkillers, and finds surprising connections. In the future, these findings could help patients with chronic pain to better manage their discomfort.

The study was carried out by researchers at Boston Children's Hospital and Beth Israel Deaconess Medical Center (BIDMC), both in Boston, MA, and their findings were published in the journal Nature Medicine.

Studying the link between sleep deprivation and pain in mice

The team - co-led by brain physiologist Alban Latremoliere, Ph.D., and sleep physiologist Chloe Alexandre, Ph.D. - investigated the impact of acute and chronic sleep deprivation, as well as the resulting sleepiness, on sensitivity to painful and non-painful stimuli.

They also examined the effect of common painkillers such as ibuprofen and morphine, alongside the effect of wakefulness-promoting drugs such as caffeine and modafinil, on pain sensitivity.

At the beginning of the study, the team monitored the sleep cycles and sensory sensitivity of between six and 12 mice using small headsets that took electroencephalography and electromyography measurements. This provided the researchers with baseline data.

The researchers then found a way to deprive the mice of sleep in a manner that was not stressful: by entertaining them. To replicate what happens when humans stay up too late, they distracted the mice with toys and fun activities when they were supposed to be asleep.

They were careful to prevent the mice from sleeping without overstimulating them. The mice were kept awake for either 12 hours straight, or for 6 hours during 5 successive days. Throughout these periods of wakefulness, the researchers monitored sleepiness, stress levels, and tested for pain sensitivity.

Sensitivity to painful stimuli was measured by applying controlled amounts of heat, cold, or pressure to the mice. Additionally, the rodents were also exposed to capsaicin - the active compound in hot chili peppers.

The researchers measured how long it took the mice to move away from the painful stimuli, or how long before they started licking away the pain caused by the hot chili compound.

Sensitivity to non-painful stimuli was tested by startling the mice with a sudden, loud noise and observing their response, which was usually to jump.

Pain killers do not work, but caffeine does

The study revealed a strong connection between sleep deprivation and pain sensitivity.

"We found that 5 consecutive days of moderate sleep deprivation can significantly exacerbate pain sensitivity over time in otherwise healthy mice. The response was specific to pain, and was not due to a state of general hyperexcitability to any stimuli."

Chloe Alexandre, Ph.D.

Probably the most surprising finding was that common painkillers seemed to have no efficacy in alleviating pain induced by sleep deprivation.

Neither ibuprofen nor morphine could prevent or stop the effects of the hypersensitivity induced by sleep loss.

However, modafinil and caffeine did not have pain-relieving properties in the mice that had slept normally.

The findings suggest that patients with chronic pain who use common painkillers may have to increase their dose if they are also sleep deprived, which may introduce side effects. Fatigue and sleep disorder often accompany chronic pain.

The researchers say that their findings may pave the way for a new type of painkiller.

"This represents a new kind of analgesic that had not been considered before, one that depends on the biological state of the animal. Such drugs could help disrupt the chronic pain cycle, in which pain disrupts sleep, which then promotes pain, which further disrupts sleep."

Clifford Woolf, study co-author

The researchers also recommend that patients with chronic pain complement their painkillers with sleep-inducing medications at night and drugs that keep them alert during the day, in an attempt to break the pain cycle.

Dr. Kiran Maski, sleep disorders specialist at BIDMC, also weighs in on the findings, saying, "Many patients with chronic pain suffer from poor sleep and daytime fatigue, and some pain medications themselves can contribute to these co-morbidities."

She adds, "This study suggests a novel approach to pain management that would be relatively easy to implement in clinical care. Clinical research is needed to understand what sleep duration is required and to test the efficacy of wake-promoting medications in chronic pain patients."

An international research team has revealed for the first time that testosterone protects males against developing asthma, helping to explain why females are two times more likely to develop asthma than males after puberty.

The study showed that testosterone suppresses the production of a type of immune cell that triggers allergic asthma. The finding may lead to new, more targeted asthma treatments.

One in nine Australians (2.5 million people) and around one in 12 Americans (25 million) have asthma, an inflammatory airway condition. During an asthma attack, the airways swell and narrow, making it difficult to breathe. In adults asthma is two times more prevalent and more severe in women than men, despite more being more common in boys than girls before puberty.

In 2016, the city of Melbourne, Australia, experienced a 'thunderstorm asthma' event that was unprecedented internationally in its scale and severity of consequences, with almost 10,000 people visiting hospitals over a two-day period. Thunderstorm asthma refers to allergic asthma thought to be initiated by an allergy to grass pollen. Many people with no history of asthma experienced severe asthma attacks.

Dr Cyril Seillet and Professor Gabrielle Belz from Melbourne's Walter and Eliza Hall Institute, with Dr Jean-Charles Guéry and his team at the Physiopathology Center of Toulouse-Purpan, France, led the study, published today in the Journal of Experimental Medicine.

Dr Seillet said hormones were speculated to play a significant role in the incidence and severity of asthma in women. "There is a very interesting clinical observation that women are more affected and develop more severe asthma than men, and so we tried to understand why this was happening," Dr Seillet said.

"Our research shows that high levels of testosterone in males protect them against the development of allergic asthma. We identified that testosterone is a potent inhibitor of innate lymphoid cells, a newly-described immune cell that has been associated with the initiation of asthma."

The research team found that innate lymphoid cells -- or ILC2s -- 'sensed' testosterone and responded by halting production of the cells.

"Testosterone directly acts on ILC2s by inhibiting their proliferation," Dr Seillet said. "So in males, you have less ILC2s in the lungs and this directly correlates with the reduced severity of asthma."

ILC2s are found in the lungs, skin and other organs. These cells produce inflammatory proteins that can cause lung inflammation and damage in response to common triggers for allergic asthma, such as pollen, dust mites, cigarette smoke and pet hair.

Professor Belz said understanding the mechanism that drives the sex differences in allergic asthma could lead to new treatments for the disease.

"Current treatments for severe asthma, such as steroids, are very broad based and can have significant side effects," Professor Belz said.

"This discovery provides us with a potential new way of treating asthma, by targeting the cells that are directly contributing to the development of allergic asthma. While more research needs to be done, it does open up the possibility of mimicking this hormonal regulation of ILC2 populations as a way of treating or preventing asthma. Similar tactics for targeting hormonal pathways have successfully been used for treating other diseases, such as breast cancer."

In a laboratory at Michigan State University, scientists took a DIY approach to build a retrofitted cryo-electron microscope that allowed them to map a giant Samba virus -- one of the world's largest viruses.

"If the common cold virus is scaled to the size of a ladder, then the giant Samba virus is bigger than the Washington Monument," said Kristin Parent, assistant professor of biochemistry and molecular biology and co-author of the paper featured on the cover of the journal Viruses. "Cryo-EM allowed us to map this virus' structure and observe the proteins it uses to enter, or attack, cells."

It seems counterintuitive that bigger organisms are harder to see, but they are when using cryo-electron microscopy. That's because these microscopes usually are used to look at thin specimens and can't decipher larger organisms to reveal their biological mechanisms. For thick samples, scientists see only dark gray or black blobs instead of seeing the molecular framework.

Cryo-EM allowed Parent's team to image the giant Samba virus and understand the structures that allow it to enter an amoeba. Once inside, Samba opens one of its capsid layers and releases its nucleocapsid -- which carries the genetic cargo that sparks an infection. While Samba isn't known to cause any diseases in humans, its cousin, the mimivirus, may be a culprit for causing some respiratory ailments in humans.

"If you scoop up a handful of water from Lake Michigan, you are literally holding more viruses than there are people on the planet," said Parent, who published the paper with Jason Schrad and Eric Young, MSU biochemistry and molecular biology graduate students. "While scientists can't study every virus on Earth, the insights we glean from viruses like the giant Samba can help us understand the mechanisms of other viruses in its family, how they thrive and how we can attack them."

As bacteria become more resistant to antibiotics, looking for new ways to fight diseases will continue to grow in importance. Parent's lab also studies how bacteria-infecting viruses enter cells using this method, which could potentially lead to new antibacterial treatments. Yet the world's best cryo-EM microscope costs more than $5 million. Limited by funds but not drive, Parent was able to upgrade an existing microscope at MSU to do cryo-EM -- one that is a tinkerer's dream.

This traditional transmission electron microscope was retrofitted with a cryostage, which keeps viruses frozen in liquid nitrogen while they're being studied. Parent and her team then added a Direct Electron DE-20 detector, a powerful camera -- the mighty microscope's piece de resistance.

Parent didn't invent cryo-EM, but establishing it on campus serves as a viable proof-of-concept for MSU, opening the door for many interdisciplinary partnerships. This cutting-edge microscopy has applications across many fields, from those addressing a single protein to others studying entire cells. Virtually anyone studying complex molecular machines can advance their work with this tool, Parent added.

Parent has earned an AAAS Marion Milligan Mason Award for Women in the Chemical Sciences. This award, her paper in Viruses and being the co-author who performed cryo-EM work in a recent Nature Communications paper, lays the groundwork to some day have a more advanced cryo-EM microscope housed at MSU to be able to perform high-resolution structural studies.

"We've done quite a bit with our limited resources, but we're primed to do more," Parent said. "I think MSU could serve as a cryo-EM center and to increase the prevalence of this technology in the Midwest and beyond."

As one example, scientists from Universidade Federal de Minas Gerais (Brazil) and Universidade Federal do Rio de Janeiro (Brazil) also contributed to this study and benefitted from the technology MSU has to offer.

A study led by Ravi Bansal, PhD, and Bradley S. Peterson, MD, of The Saban Research Institute of Children's Hospital Los Angeles, has found structural differences in the cerebral cortex of patients with depression and that these differences normalize with appropriate medication. The study, published in Molecular Psychiatry on March 7, is the first to report within the context of a randomized, controlled trial, the presence of structural changes in the cerebral cortex during medication treatment for depression and the first to provide in vivo evidence for the presence of anatomical neuroplasticity in human brain.

"Our findings suggest that thickening of the cerebral cortex is a compensatory, neuroplastic response that helps to reduce the severity of depressive symptoms," said Peterson, director of the Institute of the Developing Mind at CHLA and professor of pediatrics and psychiatry at the Keck School of Medicine of the University of Southern California. "Patients off medication have a thickened cortex, and the thicker it is, the fewer the symptoms they have. Treatment with medication then reduces the severity of symptoms, which in turn reduces the need for biological compensation in the brain -- so that their cortex becomes thinner, reaching thickness values similar to those in healthy volunteers."

The investigators acquired anatomical brain scans at baseline and again at the end of the 10-week study period for 41 patients with chronic depression, while 39 healthy volunteers were scanned once. This study was conducted with adult patients treated at Columbia University, when Peterson and Bansal were faculty members.

Patients were randomized to receive active medication duloxetine, a selective serotonin and norepinephrine reuptake inhibitor, or placebo. During the trial, patients receiving medication experienced significant improvement of symptoms compared with patients receiving placebo. In medication-treated patients, cortical thickness declined toward values found in healthy volunteers while placebo-treated patients showed a slight thickening of the cortex. According to Bansal, a researcher at CHLA and professor of pediatrics at the Keck School of Medicine of USC, this finding suggests that placebo-treated patients continue to require compensation for their ongoing symptoms.

"Although this study was conducted in adults, the methodology developed -- pairing a randomized controlled trial with MRI scanning -- can be applied to many other populations in both children and adults," said Bansal. "Also, our observations of neuroplasticity suggest new biological targets for treatment of persons with neuropsychiatric disorders."

Advanced technologies provide researchers with new insights into the warning signs for cardiovascular disease.

Screening methods for cardiovascular diseases such as heart attacks and strokes could be improved by measuring different biological signposts to those currently being tested, a new study led by researchers from King's College London suggests.

Published in the Journal of the American College of Cardiology, the study could allow doctors to better predict the development of cardiovascular disease at an earlier stage.

The research, which was supported by the National Institute for Health Research (NIHR) Biomedical Research Centre at Guy's and St Thomas' NHS Foundation Trust and King's College London, explored the role of a family of proteins called apolipoproteins.

Currently, the main focus is on apolipoprotein A1 (apoA1), the main component of high-density lipoproteins (HDL) or 'good' cholesterol, and apolipoprotein B (apoB), which is present on low-density lipoproteins (LDL) or 'bad' cholesterol.

However, for the first time, researchers have used a technology called mass spectrometry to measure an unprecedented number of apolipoproteins in a population-based study and discovered that another group of apolipoproteins might complement the signposts of good and bad cholesterol: apoE, apoC2 and apoC3.

These apolipoproteins are associated with very low-density lipoproteins (VLDL) and predominantly linked to another type of fat called triglycerides. ApoE, apoC2 and apoC3 have shown a stronger association with cardiovascular disease than apoA1 and apoB, suggesting that currently some of the most predictive apolipoproteins are not measured in patients who may be at risk of cardiovascular disease.

The findings could lead to a change in the way patients all over the world are screened for cardiovascular disease, a condition which affects seven million people and causes more than 160,000 deaths in each year in the UK. It could also pave the way for more personalised treatments.

Lead author of the study Professor Manuel Mayr from King's College London said:

"We directly compared the association of a broad panel of apolipoproteins to new onset of cardiovascular disease over a 10-year observation period, and found that while apoB was predictive, other apolipoproteins, namely apoE, apoC2 and apoC3, were even better.

"These unexpected strong associations of VLDL-associated apolipoproteins with cardiovascular disease provide support to expanding the current measurements of apolipoproteins and to the concept of targeting additional apolipoproteins to reduce risk."

The study identified apoC3 as a prime therapeutic target for lowering VLDL, which might reduce excess cardiovascular risk related to high VLDL.

After all the lifting, hauling and wrapping, worn out gift givers may blame the season's physical strain for any shoulder soreness they are feeling. It turns out there could be another reason. A new study led by investigators at the University of Utah School of Medicine finds that individuals with symptoms that put them at increased risk for heart disease could be more likely to have shoulder problems, including joint pain and rotator cuff injury.

"If someone has rotator cuff problems, it could be a sign that there is something else going on. They may need to manage risk factors for heart disease," says the study's lead author Kurt Hegmann, M.D., M.P.H., Professor of Family and Preventive Medicine and Director of the Rocky Mountain Center for Occupational and Environmental Health. The research was published in the Journal of Occupational and Environmental Medicine.

Repeated physical stress is most frequently blamed for aggravating shoulder joints and the muscles and tendons that surround them. Think about a pitcher who throws a baseball 100 times a day. While physical exertion can certainly be an irritant, accumulating evidence points other factors that could also be at play. Previous research found that people who had an increased risk for heart disease also had a tendency toward carpal tunnel syndrome, Achilles tendinitis, and tennis elbow, all musculoskeletal disorders.

The current study by Hegmann and colleagues adds shoulder problems to the list and takes the connection one step further. The more heart disease risk factors that each of the study participants had racked up -- including high blood pressure, high cholesterol, diabetes -- the more likely they were to have had shoulder trouble.

36 participants with the most severe collection of risk factors were 4.6 times more likely than those with none of the risk factors to have had shoulder joint pain. They were also nearly six times more likely to have had a second shoulder condition, rotator cuff tendinopathy. Participants with mid-level heart risk were less likely to have had either shoulder condition, at 1.5 to 3-fold. Shared trends bolster that there could be a relationship between heart risk and shoulder problems, but researchers will need to follow up with a prospective study to prove cause and effect.

It may seem like physical strain would be at least just as likely to cause shoulder pain but data from the 1,226 skilled laborers who took part in the study suggest otherwise. Ergonomists carefully monitored airbag manufacturers, meat, processors, cabinet makers and skilled laborers. Every forceful twist, push, and pull was factored into a strain index assigned to each worker. But a more straining job did not translate to an uptick in shoulder difficulties. Nor did more time spent doing other physical activities.

"What we think we are seeing is that high force can accelerate rotator cuff issues but is not the primary driver," says Hegmann. "Cardiovascular disease risk factors could be more important than job factors for incurring these types of problems."

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In Sancti Spiritus People also Shouted ´I am Fidel´

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Cubasí.cu interviewed translator Aracelia del Valle from Escambray website on people’s reaction for the journey of the caravan carrying the remains of Commander in Chief Fidel Castro to Santiago de Cuba.